Haemostasis Lecture Notes PDF
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Uploaded by FineLookingAquamarine248
LSBU
Gulshana Choudhury
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Summary
This lecture covers the process of haemostasis, including clotting cascade, clot retraction, and fibrinolysis. The relevance of haemostasis to dental procedures is also discussed. The document includes diagrams and figures.
Full Transcript
Haemostasis Tutor: Gulshana Choudhury Module: Biomedical Sciences GDC Learning outcomes 1.1.3 Explain general and systemic disease and their relevance to oral health 1.1.6 Describe relevant and appropriate physiology and explain its application to patient management 1.1.8 Describe th...
Haemostasis Tutor: Gulshana Choudhury Module: Biomedical Sciences GDC Learning outcomes 1.1.3 Explain general and systemic disease and their relevance to oral health 1.1.6 Describe relevant and appropriate physiology and explain its application to patient management 1.1.8 Describe the properties of relevant medicines and therapeutic agents and discuss their application to patient management Learning outcomes Describe the process of haemostasis and clot formation Describe the clotting cascade and the significance of clotting factors Outline the relevance of haemostasis to the dental hygienist/therapist What is haemostasis? The process by which bleeding stops When a blood vessel is damaged a number of overlapping processes occur to stop bleeding Why is haemostasis important? Blood is an important connective tissue Keeps all organs nourished If we are injured, it is important that blood loss is stopped as quickly as possible Consequences of rapid blood loss Minor loss Moderate loss Body’s homeostatic mechanisms Headache maintain blood volume and cells Fatigue Nausea Sweating Dizziness Consequences of rapid blood loss Severe loss Clammy, cold, pale skin Rapid, shallow breathing, rapid heart rate Little or no urine output Confusion Weakness Weak pulse Blue lips and fingernails Light-headedness Loss of consciousness Death Stages of haemostasis 1.Vasoconstriction 2. Platelet plug 3. Coagulation formation Primary haemostasis Secondary haemostasis Primary haemostasis 1. Vasoconstriction Initial bleeding stopped by constriction of blood vessels Platelets adhere to damaged wall Platelets release serotonin (5-HT) and thromboxanes Smooth muscle in vessel wall contracts Other vasoconstrictors e.g. endothelins are released by damaged vessel Primary haemostasis 2. Platelet plug Platelets clump together around exposed collagen fibres Process is assisted by a glycoprotein in the blood plasma called von Willebrand factor – stablises platelet plug Platelets release chemicals e.g. adenosine diphosphate (ADP) which attracts other platelets to site Formation of platelet plug Bleeding time The time taken for primary When is bleeding time haemostasis (blood vessel prolonged? constriction and platelet plug Thrombocytopaenia, severe formation) to occur anaemia, collagen disorders e.g. Ehlers Danlos syndrome, Von Willebrand’s disease 2-7 minutes Anti-platelet drugs e.g. aspirin, clopidogrel Secondary haemostasis 3. Coagulation Platelets Red/white blood cells Complex process resulting in Fibrin platelet plug being stabilised by insoluble fibrin strands forming a mesh Clot Fibrin is formed from the soluble fibrinogen through the clotting cascade Fibrin mesh Clotting cascade Extrinsic pathway (tissue factor pathway) Main pathway Triggered by Tissue factor (factor III) released by damaged endothelial cells Tissue factor converts factor VII to factor VIIa Factor VIIa goes on to activate factor X into factor Xa Extrinsic Pathway Thereafter common pathway measured by Prothrombin Time (PT) Normal value = 11-16 seconds Intrinsic pathway (contact pathway) Triggered by blood coming into contact with collagen fibres in the broken wall of a blood vessel “Intrinsic" because it's initiated by a factor inside the blood vessel Starts with activation of factor XII (serine protease) which becomes factor XIIa after exposure to Intrinsic Pathway measured endothelial collagen after damage. by Activated Partial Thromboplastin Time Ends with common pathway (aPTT) Normal value = 23-35 seconds Common pathway Prothrombin is converted to thrombin (serine protease) Thrombin converts the soluble fibrinogen into fibrin strands Factor XIII acts on fibrin strands to form a fibrin mesh Coagulation factors Majority are synthesised in the liver Factor VII is created by the vascular endothelium Vit K essential for formation of clotting factors in the liver Liver pathology can cause problems with forming clotting factors Inherited disorders such as Haemophilia A, B and C lead to a lack of factor VIII, IX and XI respectively Effects of anticoagulants on the clotting cascade Anticoagulan Indications: ts are drugs Atrial that help fibrillation prevent Deep vein blood from thrombosis clotting Stroke Drugs such as Warfarin, Heparin and Rivaroxaban block different parts of the clotting cascade Summary of the coagulation cascade Clot retraction Contraction of approximately 90% of initial clot volume within 24 hours Actin and myosin proteins within activated platelets pull clot tight Fibrin threads draw more closely together Serum exudes Clot shrinkage pulls the edges of the damaged vessel together, reducing blood loss Clot breakdown – fibrinolysis Plasminogen, trapped within the clot is converted to plasmin Plasmin breaks down fibrin Thrombin activated fibrinolysis inhibitor (TAFI) is a fibrinolysis inhibitor and stabilises clots Fibrinolysis – abnormalities Fibrinolysis enhanced by Fibrinolysis depressed by Disseminated intravascular Alcoholic liver disease coagulation Antiphospholipid syndrome Metastatic prostate cancer Hypothyroidism Chronic renal disease Pregnancy Thrombosis Caused by: 1. Over-activity of coagulation 2. Under-activity of fibrinolysis Most often starts at an area of vascular endothelial damage to which platelets adhere Dental relevance Dental procedures cause haemorrhage Bleeding should stop naturally after 4-10 min depending on wound Separate lecture on the many causes of prolonged bleeding and how to manage it Haemorrhage in dentistry Controlled in dentistry by: Pressure Sutures Packing with haemostatic agents e.g. Surgicel Less commonly: Electrosurgery unit – coagulation wavelength Lasers Summary Described the process of haemostasis and clot formation Described the clotting cascade and the significance of clotting factors Briefly described clot retraction and fibrinolysis Outlined the relevance of haemostasis to the dental hygienist/therapist Quiz https://forms.office.com/e/4Gwp2jucNm Further reading Haemostasis revealed. Available at: https://www.youtube.com/watch?v=-F73CMjVuqg Haemostasis revealed. Available at: https://www.youtube.com/watch?v=-F73CMjVuqg SDCEP Management of Dental Patients Taking Anticoagulants or Antiplatelet Drugs (second edition) 2022. Available at https://www.sdcep.org.uk/media/ypnl2cpz/sdcep-management-of-dental- patients-taking-anticoagulants-or-antiplatelet-drugs-2nd-edition.pdf